This binding leads to the recruitment of the adaptor protein myeloid differentiation primary response protein 88 (MyD88) to the cytoplasmic domain of TLR4, resulting in the activation of the transcription factor NF-κB (Liu et al., 2017) and the expression of NLRP3, GSDMD, and IL-1 in downstream inflammatory pathways, ultimately promoting HF development (Violi et al., 2023). The gene discussed is MYD88; the disease is hydrops fetalis.